Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The activities of monoamine biosynthetic enzymes were measured in brain regions of several hypertensive rat models at various ages. The types of hypertensive rats were the spontaneously hypertensive rat (SHR) and a stroke-prone substrain of the SHR as well as DOCA-salt and renal hypertensive rats. The genetically hypertensive rats had significantly elevated blood pressures as compared to the Wistar-Kyoto control rat after 5 weeks of age. During the early development of hypertension in the SHR, the activities of tyrosine hydroxylase in the hypothalamus and corpus striatum and of dopamine-beta-hydroxylase in the hypothalamus and pons-medulla were significantly higher than in the control rats. Tryptophan-hydroxylase was also elevated in the hypothalamus in SHR. From 3 to 8 weeks of age there appeared to be a significant correlation between hypothalamic dopamine-beta-hydroxylase activity and blood pressure in the hypertensive rats. In contrast, the activities of tyrosine hydroxylase and dopamine-beta-hydroxylase were slightly decreased in the DOCA-salt and renal hypertensive rats. It is suggested that noradrenergic or adrenergic neurons in the hypothalamus may participate in the initiation of elevated blood pressure in the genetic, but not in the DOCA-salt or renal hypertensive rats.
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PMID:Regional changes in the activities of aminergic biosynthetic enzymes in the brains of hypertensive rats. 1 54

The acute and intermediate onset phases of one-clip, two-kidney hypertension were studied in six conscious dogs. Mean arterial pressure (MAP), cardiac output (CO), total peripheral resistance (TPR), serum renin concentration (SRC), plasma aldosterone (PA) and cumulative sodium and water balance were studied prior to unilateral renal artery constriction, at 2, 10, and 24 hours postconstriction, and daily thereafter for 5 days. At 2 hours postconstriction, MAP, CO, TPR, and SRC were elevated, with unchanged fluid balance. At 10 and 24 hours there was a further rise in CO accompanied by positive fluid-sodium balance, with a slight decrease in MAP, TRP, and SRC. During days 2 and 3, MAP, CO, TPR, and SRC remained elevated and stable in the presence of decreasing fluid-sodium balance to preconstriction levels. During days 4 and 5, MAP, SRC, and fluid-sodium balance remained unchanged, TPR demonstrated a secondary increase, whereas CO decreased to preconstriction values. Sequential changes in PA parallel those of SRC, but were significant only at 2 hours postconstriction. These changes suggest that the increased CO is not totally dependent on fluid-sodium balance, and that CO is not the sole determinant of elevated MAP. The temporal relationship between MAP and SRC throughout the study is consistent with renin-mediated hypertension. The secondary rise of TPR may be due to total body autoregulation and/or increased vascular reactivity to high levels of circulating angiotensin. A unitary renin-angiotensin mechanism, therefore, may be responsible for the induction and maintenance of hypertension in this experimental model.
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PMID:Mechanisms of hypertension during the acute and intermediate phases of the one-clip, two-kidney model in the dog. 87 Feb 28

We studied the effect of indole-3-pyruvic acid (IPA) on systolic blood pressure of normotensive, spontaneously hypertensive, DOCA + salt hypertensive, and Grollman hypertensive rats. Experiments were also carried out in order to investigate whether IPA may influence the development of hypertension in spontaneously hypertensive rats. Age-matched normotensive, spontaneously hypertensive, DOCA + salt hypertensive, and Grollman hypertensive rats treated with N-methylglucamine, were used as controls. Acute oral (up to 50 mg/kg) and intravenous (5 mg/kg) administration of IPA did not change systolic blood pressure in any models of hypertension. By contrast, a repeated administration of IPA (100 mg/kg/day, by oral gavage for 10 days) significantly decreased systolic blood pressure in all models of hypertension, while it elicited no significant effect in normotensive rats. Moreover, when IPA was given daily to 5-week-old spontaneously hypertensive rats for 7 weeks, it partially inhibited the development of hypertension. In addition, chronic administration of IPA caused enhanced levels of tryptophan and 5-hydroxyindoleacetic acid in the cortex and diencephalon. Brainstem serotonin content in both normotensive and spontaneously hypertensive rats was also enhanced by IPA treatment. Our results suggest that IPA lowers blood pressure in different rat models of hypertension and this effect seems to be correlated with an increase in cerebral serotonin metabolism.
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PMID:Antihypertensive activity of indolepyruvic acid: a keto analogue of tryptophan. 168 65

A number of reports of potential etiologic agents of localized and systemic scleroderma appeared in the past year, including alterations in tryptophan metabolism, use of appetite suppressants, and exposure to silicone. An infectious agent, Borrelia burgdorferi, was found not to be implicated in localized scleroderma. The improvement in outcome of systemic scleroderma complicated by renovascular hypertension was highlighted in several papers, as was the emerging importance of cardiac and pulmonary involvement. Recent advances in the early detection and evaluation of cardiac and pulmonary complications of scleroderma are discussed.
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PMID:Clinical aspects of localized and systemic scleroderma. 177 53

The effects of tryptophane on growth and hypertension of offspring obtained from mothers given L-tryptophane prior to mating: In the tryptophane group, body weights were heavier and blood pressures were higher than in the control group. Stroke lesion incidence rates were also much higher in the tryptophane group. At 20 weeks of age, brain enzyme activities were lower and serotonin content was higher in the tryptophane group in comparison with the control. These results suggest that dietary tryptophane may affect precocious maturation and as well as affect elevation in blood pressures due to brain serotonin turnover.
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PMID:Effects of tryptophane on SHRSP offspring growth. 177 28

This study was designed to assess the effect of chronic dietary administration (2.5 and 5.0% by weight) of the neutral amino acid, L-tryptophan, on the development of hypertension during chronic exposure to cold. In addition, a warm-adapted and cold-treated control group receiving unsupplemented food were used. Chronic administration of the lower dose of L-tryptophan (850 mg/day) prevented the elevation of blood pressure attenuated cardiac hypertrophy, and had no effect on body weight during exposure to cold. The higher dose of L-tryptophan (1,690 mg/day) attenuated the rate of blood pressure increase, did not affect cardiac hypertrophy, attenuated the gain in body weight, and increased the urinary output of epinephrine. Thus, this dose may be associated with some toxicity. Both doses of tryptophan failed to prevent certain other responses characteristically occurring during exposure to cold: i.e. increased weight of the kidneys, adrenal glands and brown adipose tissue; increased food and water consumption; increased dipsogenic responsiveness to angiotensin II, and increased plasma aldosterone concentration. The results indicate that chronic dietary administration of L-tryptophan (850 mg/day) can prevent the development of cold-induced hypertension, as it can in all other models of hypertension tested thus far in rats.
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PMID:Effect of chronic dietary treatment with L-tryptophan on the development of cold-induced hypertension in rats. 194 99

Dahl salt-sensitive rats are inbred on the basis of their tendency to develop hypertension when placed on a high salt diet. The present study investigated the effects of chronic dietary tryptophan (trp) at 50 g/kg food on the development of hypertension in these animals under conditions of both normal and elevated dietary salt. Dietary trp attenuated the development of hypertension in inbred Dahl salt-sensitive (DS/JR) rats and had no effect upon the patterns of development of systolic blood pressures in the normotensive controls, the inbred Dahl salt-resistant (DR/JR) rat and the outbred parental Sprague Dawley (SD) rat. Cardiac hypertrophy, which is associated with Dahl salt-induced hypertension, was blocked by the high trp diet. Further work will be necessary to elucidate the mechanisms by which dietary trp protected against the development of hypertension and cardiac hypertrophy in DS/JR rats.
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PMID:Effect of dietary tryptophan on the development of hypertension in the Dahl salt-sensitive rat. 213 37

Scleroderma developed in six women who were taking L-tryptophan. Fasciitis and morphea were most common, but one patient had pleural effusion, hypertension, and signs of cardiac and kidney failure. In five patients the biopsy findings were characteristic of scleroderma; the sixth patient had Crohn's disease and developed fasciitis; her biopsy specimen showed inflammatory arteritis. All patients' conditions improved after cessation of their L-tryptophan intake, initiation of corticosteroid therapy, or both. These findings confirm previous data that show altered tryptophan-kynurenine metabolism in some patients with scleroderma and fasciitis, particularly with tryptophan loading.
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PMID:Scleroderma and L-tryptophan: a possible explanation of the eosinophilia-myalgia syndrome. 221 43

Four-week-old inbred Dahl salt-sensitive (DS/JR) and Dahl salt-resistant (DR/JR) rats were placed on an 8% salt diet with or without a supplemental 2.5% tryptophan (Trp). Blood pressures were monitored for the next 5 weeks. Urine volumes and ion concentrations were measured during the 6th week. Blood pressures of DS/JR rats on control diets elevated rapidly and markedly, whereas pressures of DS/JR rats on the Trp-supplemented diet were not significantly elevated over those of DR/JR rats. Pressures of DR/JR rats were unaffected by Trp supplementation. Urinary sodium was significantly greater in DR/JR rats compared with DS/JR rats and was unaffected by Trp supplementation. This suggests that the antihypertensive effect of Trp was not at the level of the kidney. We conclude that dietary Trp blocks the development of hypertension in DS/JR rats maintained on a high salt diet.
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PMID:Prevention of Dahl salt-induced hypertension by chronic dietary tryptophan. 228 87

Hypotensive responses to tryptophan and 5-hydroxytryptophan infusions were studied in normotensive male Sprague-Dawley rats. Results showed that 5-hydroxytryptophan but not tryptophan lowered pressure in a dose dependent way in direct relation to the production of brain serotonin and 5-HIAA. Intrinsic release of serotonin from brain was also studied during periods of induced hypertension and hypotension. Brain monoamine responses to blood pressure changes induced by intravenous phenylephrine and nitroprusside were measured in dorsal raphe nucleus and nucleus tractus solitarius by in vivo electrochemistry. Results showed that 5-HIAA was increased during drug induced hypertension and during reflex hypertension which followed a period of hypotension. These changes were blocked by sinoaortic denervation indicating that these central serotonergic neurons are responding to increased pressure sensed by baroreceptors. Therefore, serotonin has a role in blood pressure regulation as a pharmacologic agent and as a neurotransmitter in homeostatic control of pressure.
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PMID:Brain serotonin and blood pressure regulation: studies using in vivo electrochemistry and direct tissue assay. 241 30


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